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August 1989

Parkinson's Disease, Vitamin E, and Mitochondrial Energy Metabolism

Author Affiliations

Department of Cell and Molecular Biology Medical College of Georgia Augusta, GA 30912

Arch Neurol. 1989;46(8):840-841. doi:10.1001/archneur.1989.00520440020007

To the Editor.  —1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes parkinsonism in humans and experimental animals by causing the death of dopaminergic striatal neurons. The ultimate toxin is thought to be a monoamine oxidase metabolite of MPTP, the 1-methyl-4-phenylpyridinium ion (MPP+), which is transported by the normal dopamine reuptake system, is concentrated by the mitochondria, and then poisons the cell by blocking the respiratory chain.1-3Several authors have presented evidence for the involvement of oxygen radical damage in the toxic effects of MPTP.4 Dopaminergic neurons accumulate lipofuscin, a hallmark of oxidative damage, after MPTP administration.5,6 Some experiments, although not all, have demonstrated amelioration of MPTP-caused dopaminergic neuron loss by prior administration of antioxidants, including vitamin E.2,7 Other data also demonstrate initiation of oxidative damage by MPTP in various systems.8-10 Moreover, the possible involvement of oxidative damage in the loss of dopaminergic neurons in idiopathic Parkinson's disease has led to

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